4.3. Biological Explanations of Sz Flashcards
What is the genetic explanation?
Trying to find a gene responsible for causing sz
What happens if we find a gene responsible for causing sz?
It could lead to early detection and prevention of sz
Twin genetic element
Gottesman: Mz twins = 48%, Dz twins = 17%
How does adoption show a genetic element?
Separates genetics from environment, Tienari (2004), found 6.7% of adoptees with a biological mother with sz.
How do candidate genes link to the genetic explanation of sz?
- There is not a ‘sz gene’ but several genes are involved.
- Sz is polygenic and aetiologically heterogenous.
- Ripke et al conducted a huge study using previous data comparing 37,000 patients data with 113,000 controls and 108 genetic variations associated with increased risk of developing sz were identified. Many coded for the dopamine neurotransmitter.
How do mutations link to the genetic explanation of sz?
- Sz can have a genetic origin without a family history due to a mutation in parental DNA.
- Evidence comes from Brown et al (2002) who found a correlation between paternal age (associated with increased risk of sperm mutation) and risk of sz
What does neural correlates mean?
Structural and functional brain abnormalities
Neural correlates are measurements of the structure or function of the brain that correlate with the +ve or -ve symptoms of sz.
What are the main steps of neural and synaptic transmission?
- Electric impulse passes along axon
- Synaptic vesicles release neurotransmitters
- Neurotransmitters pass into synapse
- Neurotransmitters bind to receptors on dendrites of a neuron
What is hyperdopaminergia?
- Original view
- Too much dopamine in the subcortex
- Central areas of the brain, including Broca’s area (responsible for speech production) -> associated with +ve symptoms such as hallucinations and delusions but also speech poverty
What is hypodopaminergia?
- Recent view
- Too little dopamine in the cortex
- The prefrontal cortex (responsible for thinking and decision making) -> associated with -ve symptoms such as avolition
Can you use both dopamine hypotheses?
They both have worth and could be correct but antipsychotics support the original view by reducing dopamine activity by blocking receptors
How does Parkinson’s Disease link to sz?
- Parkinson’s sufferers have low levels of dopamine.
- L-dopa raises DA activity
- People with Parkinson’s develop schizophrenic symptoms if they take too much L-dopa
- Chlorpromazine (given to schizophrenics) reduces the symptoms by blocking D2 receptors.
Strength: strong evidence base for genes
- Gottesman family study shows how genetic similarity and shared risk of sz are closely related
- Adoption studies Tienari (2004) show biological children of people with sz are still at heightened risk of sz even if adopted into a family without a history of sz
- Hiker et al (2018)- 33% concordance for Mz and 7% for Dz twins
- This shows that some people are more vulnerable to sz because of their genes
Strength: Support for dopamine (neural correlates)
- Tauscher et al (2014) also showed antipsychotics that reduce DA also reduce intensity of symptoms
- Amphetamines increase DA and mimic sz symptoms
- This strongly suggests that dopamine is involved in symptoms of sz
Weakness: evidence for environmental risk factors (genes)
- Biological risk factors include birth complications (Morgan et al 2017) and smoking THC-rich cannabis in teenage years (Di Forti et al 2015)
- Psychological risk factors include childhood trauma e.g. 67% with sz (38% matched controls) reported at least one childhood trauma (Morkved et al 2017)
- This means that genes alone cannot provide a complete explanation for sz
